Vancomycin Trough and Acute Kidney Injury: A Large Retrospective, Cohort Study

Abstract

Background: The association between vancomycin trough (VT) and acute kidney injury (AKI) at the recommended doses remains controversial. Methods: The authors conducted a retrospective, observational cohort study of 500 adult patients who received vancomycin for ≥72 h. Data collected included 2 main predictors: average VT (including only VTs before the occurrence of AKI), first VT and other possible risk factors for AKI. The baseline characteristics/variables between patients with AKI and patients with no AKI were compared. Logistic regression models were used to develop multivariate models. The authors divided the patients into 4 subgroups: (1) VT <10, (2) 10 ≤ VT < 15, (3) 15 ≤ VT < 20 and (4) VT ≥20 µg/ml. All subgroups were compared to subgroup 2 (reference group). Results: AKI occurred in 12.85% of patients while on vancomycin. The incidence of AKI in subgroups 1-4 was 8.02, 13.61, 13.70 and 31.82%, respectively, using the first VT, that is significantly higher in subgroup 4. Using average VT, AKI incidence was 5, 10.38, 19.01 and 25.58%, respectively, that is significantly higher in subgroups 3 and 4. On multivariate logistic regression, average VT, first VT, average VT >15, first VT >15, methicillin-resistant Staphylococcus aureus infection and morbid obesity were significantly associated with increased incidence of AKI. Conclusion: Clinicians should be careful when aiming for a VT >15 μg/ml as this is associated with increased incidence of AKI.

Incidence of Acute Kidney Injury Among Patients Receiving the Combination of Vancomycin with Piperacillin‐Tazobactam or Meropenem

“…Another study assessing the risk of AKI with VAN/PTZ versus VAN/CEF revealed a greater risk of developing AKI with VAN doses between 3 and 4 g/day, but not with doses 4 g/day or greater (OR 1.6, CI 1.11–2.32, p=0.01, and OR 1.3, CI 0.5–3.05, p=0.6, respectively) . Steady‐state VAN trough concentrations of 15 μg/ml or greater were associated with a greater risk of developing AKI in several studies . Independent risk factors identified in other studies included dehydration, patient weight, concomitant use of acyclovir, amphotericin B, or loop diuretics, duration of VAN treatment 7 days or longer, longer duration of hospital stay, receipt of VAN loading dose, presence of two or more systemic inflammatory response syndrome criteria, and a documented gram‐positive infection …”

“…9 Steady-state VAN trough concentrations of 15 lg/ml or greater were associated with a greater risk of developing AKI in several studies. 10,22,33,[39][40][41][42][43][44][45] Independent risk factors identified in other studies included dehydration, patient weight, concomitant use of acyclovir, amphotericin B, or loop diuretics, duration of VAN treatment 7 days or longer, longer duration of hospital stay, receipt of VAN loading dose, presence of two or more systemic inflammatory response syndrome criteria, and a documented gram-positive infection. 9,22,24,31,39 Baseline characteristics, specifically the significantly higher mean Charlson Comorbidity Index in the MER group, may indicate a higher severity of illness than those who received PTZ.…”

MBD2 upregulates miR-301a-5p to induce kidney cell apoptosis during vancomycin-induced AKI

“… 1 , 2 The recent study confirmed that prevalence of MRSA with reduced susceptibility to VAN was gradually increased, which prompted specialists to recommend for higher target trough serum concentrations. 3 , 4 , 5 However, the use of larger doses of VAN has led to a wider report of acute kidney injury (AKI) cases. 6 , 7 Although the most of them are mild or even reversible, both the greater incidence of end-stage renal disease (ESRD) and higher mortality rate may be associated with their germination.…”

Vancomycin associated acute kidney injury in pediatric patients

“…Both of these mean values have a wide standard deviation and are considerably lower than the often cited 15 mg/L for prevention of vAKI. [ 12 , 21 , 32 – 34 ] We sought to minimize the concerns of causation versus outcome by collecting serum vancomycin concentrations in the 72 hours prior to vAKI, and to collect values at particular times after a dose, rather than a trough concentration, to capture data from those patients who may have been receiving non-scheduled vancomycin dosing due to real or perceived pre-existing kidney dysfunction. [ 20 ] Therefore, we were unable to evaluate serum concentrations at specifically at steady state, and values sampled at steady state may be different than what we have been able to capture.…”